The exact cause of prostate cancer is unknown, but medical professionals generally agree that both genetics and environment play a role, with the larger focus on genetics. Prostate cancer occurs when mutant prostate gland cells begin to multiply and spread beyond the prostate gland, unchecked by the genes that normally act to prevent them.
Tumor Suppressor Genes vs. Oncogenes
Tumor suppressor genes control when our cells grow, divide into new cells, and die. Oncogenes, on the other hand, help cells grow, divide, and stay alive. Prostate cancer occurs when either of these types of cells fail to perform in their normal fashion, as directed by the endocrine system. These prostate-cancer susceptibility genes, and their unique mutations, are either inherited (primarily from a parent) or acquired during a man’s lifetime as a result of inflammation, hormone levels, radiation, or even diet.
In effect, men whose family members have (or have had) prostate cancer carry cancer susceptibility genes, and are as a result more likely to develop prostate cancer. This prostate cancer risk increases, from 3.14 percent among brothers (i.e., those diagnosed with prostate cancer before age 65), to 4.39 percent where two or more family members are diagnosed with prostate cancer at any age. Inherited genes contributing to prostate cancer include:
• RNASEL, which is largely responsible for cell death, or aptosis. When RNASEL fails, normal cells may continue to survive even when they become a threat (i.e., no longer able to modify their behavior), and defective cells not only persist, but also spread.
• BRCA1 and BRCA2, the tumor suppressor genes, which normally help prevent or repair damaged cells, or cause the cells to die if they can’t be repaired. These two account for a very small but significantly persistent portion of prostate cancers, and a much larger proportion of breast and ovarian cancers in women.
• MLH1, MSH2, MSH6, and PMS2, or EPCAM, are repair genes that normally help repair mistakes in DNA when the cell is duplicating its DNA prior to dividing and – just like “debugging” computer hardware or software operating codes – the process sometimes fails, particularly as the system gets older, as is the case with prostate cancer.
• Men who inherit defective, or mutated, MSH2 and MLH1 genes are said to have Lynch Syndrome (hereditary nonpolyposis colorectal cancer, or HNPCC). They are, as a result, more likely to develop prostate cancer, colorectal cancers, and stomach cancer, as well as cancers of the liver, gallbladder ducts, upper urinary tract, brain and skin.
• There may also be other inherited gene mutations that account for some cases of hereditary prostate cancer, and researchers continue to explore the possibilities.
Acquired Prostate Cancer Risk Factors
Certain factors (inflammation, hormone levels, radiation, or even diet) may also cause genetic mutations or irregularities that contribute to prostate cancer. For example, men with high levels of androgens, or male hormones like testosterone, may produce more cells than normal, and this excess itself leads to prostate cancer.
High levels of insulin-like growth factor-1 (IGF-1), needed for cell growth rather than blood sugar metabolism, may also create a situation where excess cells lead to prostate cancer.
Additional prostate cancer causes include exposure to radiation, certain chemicals, foods, and even certain vitamins or – more importantly, dietary supplements. Potentially carcinogenic (cancer-causing) chemicals include pesticides, chlorine, steroids, arsenic, cadmium, and perfluoroctanoic acid, to name a few. Foods to avoid include red meat, cow’s milk, and other forms of calcium. Supplements containing creatine or androstenedione should be avoided.